To beat this, those on the other side of the 40s would have to clock extra hours on the treadmill and eat more salads than their younger counterparts in order to shed weight, said the research published in The FASEB Journal.

"Our brown fat stops working as we age. Unfortunately, until a way to turn it back on is developed, we would have to be prepared to eat more salads and lean proteins, while logging more miles on the treadmill than our younger counterparts," said Gerald Weissmann, editor-in-chief of The FASEB Journal that published the study.

To make this happen, scientists analysed two groups of mice. They knocked out the platelet-activating factor receptors (PAFR) gene in first group. The second group was normal.

PAFR-deficient mice developed a more severe obese state characterised by higher body and epididymal fat mass with age than that of the normal group.

"The research revealed that PAFR-deficiency causes brown adipose tissue (BAT) dysfunction - which converges to induce the development of obesity - due to impaired thermogenic activity of BAT," said Junko Sugatani, a researcher at school of pharmaceutical sciences at University of Shizuoka in Shizuoka, Japan.

Additionally, the researchers also discovered a possible metabolic on/off switch that could reactivate brown fat, said the study.

This breakthrough could elucidate the molecular mechanism underlying the PAF/PAF receptor-mediated anti-obesity, leading to the development of new targets for the treatment of obesity and related disorders, such as diabetes, high blood pressure, heart disease, cancer, infertility and ulcers, concluded the study.

End.

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